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Accuracy of "Sensitive Rapid Troponin T" Assay at Admission Point of Care in Predicting Outcome of Patients with Unstable Angina (UA)
Kazmi Khawar, Dodani Sunita
Department of Medicine and Department of Family Medicine
The Aga Khan University Hospital
Troponin T (Tn T) as a marker of myocardial cell injury has been shown to be a reliable predictor of outcome in patients (pts) with UA. Availability of rapid assay qualitative bed side kit for detection of TnT (cut off 0.2 ng/ml) has greatly enhanced its usefulness. In this study a new, more sensitive (cut off 0.1 ng/ml) bed side kit was utilized at admission in the Emergency Room (ER), to prognosticate the outcome of pts with UA.
Dec 96-Feb 97, 196 pts presented to ER with Acute Coronary Syndromes (ACS) of which 102 were admitted with either Acute Myocardial Infarction (AMI) or UA. 94 were transferred to other hospitals due to non availability of appropriate beds. Of the 36 pts admitted as UA, 1 was excluded because of incomplete sampling of CK and TnT. 35 consecutive pts with UA all had two sensitive TnT assays done 4 hrs apart in the ER. Due to pt and physician bias revascularization was not analysed as a major adverse event.
The significantly high positivity of the first TnT sample (73%)
compared to Western experience possibly relates to time delay of pt presentation in our
third world setting. However, use of more sensitive assay may have contributed as well.
Despite this, the high specificity was not compromised, maintaining a high negative
It appears that sensitive TnT assay results obtained at the initial point of care are highly predictive of outcome and could be utilized for triage of such pts to appropriate level of care thus providing optimal utilization of scarce resources.
Early rise assessment is important in patients with unstable coronary
artery disease, i.e, unstable angina or non-Q wave myocardial infarction (MI) patients
with UA or acute non-Q-wave myocardial infarction (MI).
Still have an elevated risk for subsequent cardiac events despite the considerable progress in treatment during the last decade1-4. However, the UA population is heterogeneous regarding both the severity of the underlying coronary artery disease and prognosis5. Therefore, early assessment of the risk for future cardiac events is important for the selection of appropriate medical treatment and optimal use of invasive procedures6.
During the last years, the new sensitive and specific biochemical markers of myocardial damage i.e, CK. MB (mass), myosin light chains and Troponin-T (TnT) have been found elevated in 30% to 50% of patients with UA7-9. The classic role of biochemical markers of myocyte damage in patients admitted with acute coronary syndromes has been retrospective confirmation of myocardial infarction. Studies of biochemical markers have concentrated on their role for early diagnosis, which although possible, is not considered diagnostically useful10-11.
Measurement of myocardial damage by newer, highly specific markers of myocardial damage is now possible, including cardiac structural proteins such as TnT12. This marker is not detectable in the normal population, is highly cardiac specific and in the setting of myocardial injury is released into the circulation slightly earlier than CK13. In the acute coronary syndrome of unstable angina, the presence of this marker in the plasma is diagnostically superior, because it identifies minor myocardial injury missed by other biochemical markers14-15. It also has prognostic significance, because if present, it identifies a subgroup of patients who are at high risk for early cardiac events14.
The purpose of the present study was to examine the prognostic value of admission TnT concentration measurement in patients with unstable angina and assess their outcome with the help of new, more sensitive (cut off 0.1 mg/ml) bed side TnT kit.
This was a double-blind single-center study of patients admitted with
the diagnosis of unstable angina (defined according to WHO criteria) to CCU at the Aga
Khan University Hospital. All had two sensitive TnT assays done 4 hrs apart in the ER with
CPK, CK-MB and myoglobin, according to the protocol. Patients remained under the care of
their admitting physician, who decided management in terms of need for further
investigation like angiography, revascularization etc. Management decisions were made by
primary physician based on clinical, ECG, and routine biochemical marker results. Results
of TnT were not disclosed to the primary physician. Positive TnT if obtained, further was
abandoned. At least 2 TnT were done before calling it a negative test.
Full clinical details of each patient was recorded on a prepared profoma. In-hospital follow-up was done through questioning from the patient, medical records and from primary physician.
Follow-up for cardiac events after discharge was done through telephone contact and in the clinics of concerned doctor. Survival status and cause of death were established for all patient in a 10 weeks follow-up.
Troponin T assay
Test was carried out with the help of qualitative handheld sensitive TnT device (cut off 0.1 mg/dl) test were done by the admitting on-call Emergency doctor, who were trained previously.
Data obtained was entered and analysed in Epi-Info programme. Base line demographic values were expressed as proportions of patients r means and standard deviations, analysis of ordinal variable were obtained through the level of significance test (P value ) with the help of fisher - exact test, and those of the continuos variable, cumulative hazard curves were computed by the Kaplan-Meier method.
Endpoints were cardiac death, Q-wave MI, Left Ventricular failure and recurrent angina. Due to patient and physician bias, revascularization was not analysed as a major end point event.
Cumulative end point statistical evaluation was performed through level of significance (P value).
Relative risk and odds ration of hard events was analysed through chi-square method.
Study was conducted from December 1996 - February 1997 (3 months). During this period, 196 patients presented to ER with acute coronary syndrome, of which 102 were admitted with either acute myocardial infarction or unstable angina (UA). 94 were transferred to other hospitals due to non availability of appropriate beds. Of the 36 patients admitted as UA, one was excluded because of incomplete sampling of CK and TnT. 35 consecutive patient with diagnosis of unstable angina, were enrolled in the study. These 35 patients were followed for 10 weeks (70 days) after the discharge from Hospital. Table 1 summarizes the base line demographic details of these patients. 15 (42-85%) patients were positive for TnT and 20 (57%) were negative (table 2). Baseline demographic values in the Troponin T positive and troponin T negative patients showed very little difference clinically between the groups except Non-QMI at the time of admission, seen in 6 patient, all in the positive group 6/15 (40%, P = 0.0041).
The significantly high positivity of the first TnT sample i.e 73% (table 2), compared to western figures possibly relates to
time delay of patient presentation in our third world setting. However, use of more
sensitive assay may have contributed as well. Despite this, the high specificity was not
compromised, maintaining a high negative predictive accuracy.
The overall finding from this study predicts that, though it should not be used as a sole discriminator of future risk, a serum troponin T will identify a subgroup of patients with unstable angina in routine clinical practice who are at increased risk of cardiac events on long term follow-up. Prospective randomized trials are required to identify optimum therapeutic strategies for this subgroup.
Table 1 shows the cumulative hazard curves for the unstable angina groups dichotomized according to troponin T status. For death, the curves begin to diverge after the 2nd day of admission, as there were three death all in the positive group in the early period (table 3). There was no death in the Troponin negative group (relative risk 2.67, P = 0.069). Twelve patient (80%) troponin T positive versus twenty (100%) Troponin T negative survived till 10 weeks of follow-up.
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